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This article was retracted on October 15, 2008. Blood, 1 July 2004, Vol. 104, No. 1, pp. 184-191. Prepublished online as a Blood First Edition Paper on March 4, 2004; DOI 10.1182/blood-2003-12-4274. This Article Full Text Full Text (PDF) Retraction (v112,p3529) All Versions of this Article: 2003-12-4274v1 104/1/184    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Matsuyama, W. Articles by Arimura, K. Search for Related Content PubMed PubMed Citation Articles by Matsuyama, W. Articles by Arimura, K. Related Collections Immunobiology Phagocytes Apoptosis Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY TNF-related apoptosis-inducing ligand is involved in neutropenia of systemic lupus erythematosus Wataru Matsuyama, Masuki Yamamoto, Ikkou Higashimoto, Ken-ichi Oonakahara, Masaki Watanabe, Kentarou Machida, Teizo Yoshimura, Nobutaka Eiraku, Masaharu Kawabata, Mitsuhiro Osame, and Kimiyoshi Arimura From the Department of Respiratory Medicine, National Minami-kyushu Hospital and the Third Department of Internal Medicine, Kagoshima University Faculty of Medicine, Kagoshima, Japan; and the Laboratory of Molecular Immunoregulation, National Cancer Institute–Frederick, Frederick, MD. Neutropenia is a common laboratory finding in systemic lupus erythematosus (SLE). However, the molecular mechanism of SLE neutropenia has not been fully explained. In this study, we examined whether TNF-related apoptosis-inducing ligand (TRAIL) is involved in the pathogenesis of SLE neutropenia using samples from SLE patients. Serum TRAIL levels in SLE patients with neutropenia were significantly higher than those of SLE patients without neutropenia and healthy volunteers. Serum TRAIL levels showed a significant negative correlation with neutrophil counts in SLE patients. The expression of TRAIL receptor 3 was significantly lower in SLE patients with neutropenia than in patients without neutropenia or in healthy volunteers. Treatment with glucocorticoids negated the decrease of TRAIL receptor 3 expression on neutrophils of SLE patients. TRAIL may accelerate neutrophil apoptosis of neutrophils from SLE patients, and autologous T cells of SLE patients, which express TRAIL on surface, may kill autologous neutrophils. Interferon gamma and glucocorticoid modulated the expression of TRAIL on T cells of SLE patients and also modulated the expression of cellular Fas-associating protein with death domain–like interleukin-1–converting enzyme (FLICE)–inhibitory protein (cFLIP), an inhibitor of death receptor signaling, in neutrophils. Thus, our results provide a novel insight into the molecular pathogenesis of SLE neutropenia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Neutropenia in systemic lupus erythematosus W. Conrad Liles, Gordon Starkebaum, and David C. Dale Blood 2004 104: 2. [Full Text] [PDF] This article has been cited by other articles: K.-J. Li, M.-C. Lu, S.-C. Hsieh, C.-H. Wu, H.-S. Yu, C.-Y. Tsai, and C.-L. Yu Release of surface-expressed lactoferrin from polymorphonuclear neutrophils after contact with CD4+T cells and its modulation on Th1/Th2 cytokine production J. Leukoc. Biol., August 1, 2006; 80(2): 350 - 358. [Abstract] [Full Text] [PDF] M. A. Cassatella, V. Huber, F. Calzetti, D. Margotto, N. Tamassia, G. Peri, A. Mantovani, L. Rivoltini, and C. Tecchio Interferon-activated neutrophils store a TNF-related apoptosis-inducing ligand (TRAIL/Apo-2 ligand) intracellular pool that is readily mobilizable following exposure to proinflammatory mediators J. Leukoc. Biol., January 1, 2006; 79(1): 123 - 132. [Abstract] [Full Text] [PDF] W. Matsuyama, H. Mitsuyama, M. Watanabe, Y. Shirahama, I. Higashimoto, M. Osame, and K. Arimura Involvement of Discoidin Domain Receptor 1 in the Deterioration of Pulmonary Sarcoidosis Am. J. Respir. Cell Mol. Biol., December 1, 2005; 33(6): 565 - 573. [Abstract] [Full Text] [PDF] M N Lub-de Hooge, E G E de Vries, S de Jong, and M Bijl Soluble TRAIL concentrations are raised in patients with systemic lupus erythematosus Ann Rheum Dis, June 1, 2005; 64(6): 854 - 858. [Abstract] [Full Text] [PDF] W. Matsuyama, M. Watanabe, Y. Shirahama, K.-i. Oonakahara, I. Higashimoto, T. Yoshimura, M. Osame, and K. Arimura Activation of Discoidin Domain Receptor 1 on CD14-Positive Bronchoalveolar Lavage Fluid Cells Induces Chemokine Production in Idiopathic Pulmonary Fibrosis J. Immunol., May 15, 2005; 174(10): 6490 - 6498. [Abstract] [Full Text] [PDF]

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